Interaction with CCNH/CDK7 facilitates CtBP2 promoting esophageal squamous cell carcinoma (ESCC) metastasis via upregulating epithelial-mesenchymal transition (EMT) progression

被引：25
作者：
Zhang, Jianguo [1 ]
Zhu, Junya [2 ]
Yang, Lei [2 ]
Guan, Chengqi [2 ]
Ni, Runzhou [2 ]
Wang, Yuchan [2 ]
Ji, Lili [2 ]
Tian, Ye [1 ]
机构：
[1] Soochow Univ, Dept Oncol, Affiliated Hosp 2, Suzhou 215000, Jiangsu, Peoples R China
[2] Nantong Univ, Dept Gastroenterol, Affiliated Hosp, Nantong 226001, Jiangsu, Peoples R China
来源：
TUMOR BIOLOGY | 2015年 / 36卷 / 09期
关键词：
C-terminal binding protein 2 (CtBP2); Cyclin H (CCNH); Cyclin-dependent kinase 7 (CDK7); Esophageal squamous cell carcinoma (ESCC); Metastasis; Epithelial-mesenchymal transition (EMT); DEPENDENT KINASE 7; NEGATIVE MODULATION; LOW EXPRESSION; CANCER; MIGRATION; PROTEIN; PHOSPHOPROTEIN; PLASTICITY; DECREASE;
D O I：
10.1007/s13277-015-3354-x
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
CtBP2, as a transcriptional corepressor of epithelial-specific genes, has been reported to promote tumor due to upregulating epithelial-mesenchymal transition (EMT) in cancer cells. CtBP2 was also demonstrated to contribute to the proliferation of esophageal squamous cell carcinoma (ESCC) cells through a negative transcriptional regulation of p16(INK4A). In this study, for the first time, we reported that CtBP2 expression, along with CCNH/CDK7, was higher in ESCC tissues with lymph node metastases than in those without lymph node metastases. Moreover, both CtBP2 and CCNH/CDK7 were positively correlated with E-cadherin, tumor grade, and tumor metastasis. However, the concrete mechanism of CtBP2's role in enhancing ESCC migration remains incompletely understood. We confirmed that CCNH/CDK7 could directly interact with CtBP2 in ESCC cells in vivo and in vitro. Furthermore, our data demonstrate for the first time that CtBP2 enhanced the migration of ESCC cells in a CCNH/CDK7-dependent manner. Our results indicated that CCNH/CDK7-CtBP2 axis may augment ESCC cell migration, and targeting the interaction of both may provide a novel therapeutic target of ESCC.
引用
收藏
页码：6701 / 6714
页数：14
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